• Vanessa R S Foletto, Maria A Martins, and Carlos R Tonussi.
• Departamento de Farmacologia, CCB, Universidade Federal de Santa Catarina, Florianópolis, Brasil.
• Anesth. Analg.. 2013 Jan 1;116(1):232-8.

BackgroundA previous study indicated that intrathecal administration of morphine reduces experimental inflammatory edema in rats by activating the nitric oxide/cyclic guanosine monophosphate pathway. This evidence supports the hypothesis that potassium channel opening may play an important role in mediating morphine's effect under such conditions.MethodsMale Wistar rats received intrathecal injections of drugs (20 μL) 30 minutes before paw stimulation with carrageenan (150 µg). Edema was measured as paw volume increase (in milliliters), and plasma leakage was measured by Evans blue dye leakage. Neutrophil migration was evaluated indirectly by myeloperoxidase assay. The inflammatory infiltration and vascular congestion were observed by histologic examination.ResultsMorphine (37 nmol) inhibited inflammatory edema, plasma leakage, and vascular congestion but had no effect on myeloperoxidase activity or neutrophil content compared with phosphate-buffered saline. Coinjection with 4-aminopyridine (10 nmol), glibenclamide (5 nmol), and dequalinium (10 pmol) reversed, but nicorandil (0.03 nmol) enhanced the effect of morphine.ConclusionsThese results support the hypothesis that the peripheral antiedematogenic effect produced by intrathecal morphine is mediated by potassium channel activation. Furthermore, this opioid effect does not involve the inhibition of acute neutrophil migration but does involve a reduction in capillary recruitment.

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